Evolutionary theory for modifiers of epistasis using a general symmetric model
- †School of Mathematical Sciences, Tel Aviv University, Tel Aviv, Israel 69978; and
- ‡Department of Biological Sciences, Stanford University, Stanford, CA 94305-5020
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Communicated by Samuel Karlin, Stanford University, Stanford, CA, October 4, 2006 (received for review May 15, 2006)
Abstract
Genetic interactions in fitness are studied by using modifier theory. The effects on fitness of two linked genes are perturbed by alleles at a third linked locus that controls the extent of epistasis in fitness between the first two. This epistasis is determined by a symmetric interaction matrix, and it is shown that a modifier allele that increases epistasis will invade when the linkage between the other two genes is sufficiently tight and these genes are in linkage disequilibrium. With linkage equilibrium among the major loci, increased or decreased epistasis may evolve depending on the allele frequencies at these loci.
Footnotes
- §To whom correspondence should be addressed. E-mail: marc{at}charles.stanford.edu
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Author contributions: U.L and M.W.F. contributed equally to this work; and U.L. and M.W.F. wrote the paper.
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The authors declare no conflict of interest.
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This article contains supporting information (SI) online at www.pnas.org/cgi/content/full/0608569103/DC1.
- Abbreviations:
- VAHW,
- viability analogous Hardy–Weinberg.
Abbreviation
- © 2006 by The National Academy of Sciences of the USA
